ArticleScience advances2026
Disrupting USP14-mediated PARP1 dynamics reinstates MIC-A/B-driven antigen-independent CD8
Article in Science advances, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers, 1 of them a synthesis that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
3 citing papers in PubMed, 1 synthesis or guideline pooled it.
- LAK to CIK continuum in glioma immunotherapy: a systematic review of efficacy and safety outcomes.Journal of translational medicine · 2026Pooled it
- Integrative multi-omics identifies PANX2 as a ferroptosis suppressor and potential therapeutic target in clear cell renal cell carcinoma.Frontiers in immunology · 2026Article
- Mechanisms of T cell activation: Integrating signaling pathways, experimental models, and therapeutic implications.EXCLI journal · 2026Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Antigen loss is a major mechanism of resistance to immunotherapy. MIC-A/B are stress-inducible ligands expressed by tumor cells that activate NKG2D on cytotoxic immune cells and mediate NKG2D-dependent tumor cell killing, yet the mechanisms underlying their reduced expression in glioma remain unclear. Using single-cell RNA sequencing and spatial transcriptomics, we investigated ectopic MIC-A/B in mouse glioma and identified USP14 as a key regulator through deubiquitinase screening. Proteomic, coimmunoprecipitation, chromatin immunoprecipitation, immunofluorescence, and ubiquitination assays characterized the interactions among USP14, PARP1, and nuclear factor, interleukin 3 regulated (NFIL3), while an intracranial tumor model combined USP14 inhibition and immunotherapy to evaluate effects on tumorigenesis and antitumor immunity. We found that MIC-A/B increased CD8
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.